Core temperature reflects the temperature of the internal organs. Proper temperature measurement is essential to diagnose and treat temperature impairment in patients. However, an accurate approach has yet to be established. Depending on the method used, the obtained values may vary and differ from the actual core temperature. There is an ongoing debate regarding the most appropriate anatomical site for core temperature measurement. Although the measurement of body core temperature through a pulmonary artery catheter is commonly cited as the gold standard, the esophageal temperature measurement appears to be a reasonable and functional alternative in the clinical setting. This article provides an integrative review of invasive and noninvasive body temperature measurements and their relations to core temperature.

The end-tidal carbon dioxide (ETCO₂) is frequently measured in cardiac arrest (CA) patients, for management and for predicting survival. Our goal was to study the PaCO₂ and ETCO₂ in hypothermic cardiac arrest patients. We included patients with refractory CA assessed for extracorporeal cardiopulmonary resuscitation. Hypothermic patients were identified from previously prospectively collected data from Poland, France and Switzerland. The non-hypothermic CA patients were identified from two French cohort studies. The primary parameters of interest were ETCO₂ and PaCO₂ at hospital admission. We analysed the data according to both alpha-stat and pH-stat strategies. We included 131 CA patients (39 hypothermic and 92 non-hypothermic). Both ETCO₂ (p < 0.001) and pH-stat PaCO₂ (p < 0.001) were significantly lower in hypothermic compared to non-hypothermic patients, which was not the case for alpha-stat PaCO₂ (p = 0.15). The median PaCO₂-ETCO₂ gradient was greater for hypothermic compared to non-hypothermic patients when using the alpha-stat method (46 mmHg vs 30 mmHg, p = 0.007), but not when using the pH-stat method (p = 0.10). Temperature was positively correlated with ETCO₂ (p < 0.01) and pH-stat PaCO₂ (p < 0.01) but not with alpha-stat PaCO₂ (p = 0.5). The ETCO₂ decreased by 0.5 mmHg and the pH-stat PaCO₂ by 1.1 mmHg for every decrease of 1° C of the temperature. The proportion of survivors with an ETCO₂ ≤ 10 mmHg at hospital admission was 45% (9/25) for hypothermic and 12% (2/17) for non-hypothermic CA patients. Hypothermic CA is associated with a decrease of the ETCO₂ and pH-stat PaCO₂ compared with non-hypothermic CA. ETCO₂ should not be used in hypothermic CA for predicting outcome.

Background: While ECLS is a highly invasive procedure, the identification of patients with a potentially good prognosis is of high importance. The aim of this study was to analyse changes in the acid-base balance parameters and lactate kinetics during the early stages of ECLS rewarming to determine predictors of clinical outcome. Methods: This single-centre retrospective study was conducted at the Severe Hypothermia Treatment Centre at John Paul II Hospital in Krakow, Poland. Patients ≥18 years old who had a core temperature (Tc) < 30 °C and were rewarmed with ECLS between December 2013 and August 2018 were included. Acid-base balance parameters were measured at ECLS implantation, at Tc 30 °C, and at 2 and 4 h after Tc 30 °C. The alteration in blood lactate kinetics was calculated as the percent change in serum lactate concentration relative to the baseline. Results: We included 50 patients, of which 36 (72%) were in cardiac arrest. The mean age was 56 ± 15 years old, and the mean Tc was 24.5 ± 12.6 °C. Twenty-one patients (42%) died. Lactate concentrations in the survivors group were significantly lower than in the non-survivors at all time points. In the survivors group, the mean lactate concentration decreased −2.42 ± 4.49 mmol/L from time of ECLS implantation until 4 h after reaching Tc 30 °C, while in the non-survivors’ group (p = 0.024), it increased 1.44 ± 6.41 mmol/L. Conclusions: Our results indicate that high lactate concentration is associated with a poor prognosis for hypothermic patients undergoing ECLS rewarming. A decreased value of lactate kinetics at 4 h after reaching 30 °C is also associated with a poor prognosis.

Background: We previously demonstrated that enhanced oxidative stress and reduced nitric oxide bioavailability are associated with unfavorable outcomes early after coronary artery bypass grafting. It is not known whether these processes may impact long-term results. We sought to assess whether during long-term follow-up, markers of oxidative stress and nitric oxide bioavailability may predict cardiovascular mortality following bypass surgery. Methods: We studied 152 consecutive patients (118 men, age 65.2 ± 8.3 years) who underwent elective, primary, isolated on-pump bypass surgery. We measured plasma 8-iso-prostaglandin F2α and asymmetric dimethylarginine before surgery and twice after surgery (18–36 h and 5–7 days). We assessed all-cause and cardiovascular death in relation to these two biomarkers during a mean follow-up time of 11.7 years. Results: The overall mortality was 44.7% (4.7 per 100 patient-years) and cardiovascular mortality was 21.0% (2.2 per 100 patient-years). Baseline 8-iso-prostaglandin F2α was associated with cardiovascular mortality (HR 1 pg/mL 1.010, 95% CI 1.001–1.021, p = 0.036) with the optimal cut-off ≤ 364 pg/mL for higher survival rate (HR 0.460, 95% CI 0.224–0.942, p = 0.030). Asymmetric dimethylarginine > 1.01 μmol/L measured 18–36 h after surgery also predicted cardiovascular death (HR 2.467, 95% CI 1.140–5.340, p = 0.020). Additionally, elevated 8-iso-prostaglandin F2α measured at the same time point associated with all-cause mortality (HR 1 pg/mL 1.007, 95% CI 1.000–1.014, p = 0.048). Conclusions: Our findings indicate that in advanced coronary disease, increased oxidative stress, reflected by 8-iso-prostaglandin F2α before bypass surgery and enhanced asymmetric dimethylarginine accumulation just after the surgery are associated with cardiovascular death during long-term follow-up